الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Primary percutaneous coronary intervention (PCI) is still the gold
standard treatment of ST-segment elevation myocardial infarction
(STEMI). It usually results in restoration of both infarct-related artery
(IRA) patency and thrombolysis in myocardial infarction (TIMI) flow III in
most patients. However, there remain a small proportion of patients who
continue to exhibit overt impairment of myocardial reperfusion despite
successful opening of the IRA. This phenomenon, which is called noreflow, occurs in up to 2% and in 8% to 11.5% of patients undergoing
elective and primary PCI, respectively.
The pathophysiology of no-reflow phenomenon involves
atherothrombotic microembolization, inflammation, activation of
neutrophils, and platelets, 8 which cause releasing of oxygen free radicals,
proteolytic enzymes, and proinflammatory mediators that can cause tissue
and endothelial damage, particularly in critically injured myocytes. In
addition, coronary microvascular spasm and reperfusion injury, as well as
genetic predisposition, may play a part in the pathophysiology of no-reflow
phenomenon. No-reflow phenomenon is indisputably associated with poor
short and long term clinical outcomes and may negate the potential benefits
of primary PCI in patients with STEMI. Early detection of no-reflow
phenomenon, which may occur within 1‐2 hours after completion of PCI, is
essential because it is associated with reduced myocardial salvage, larger
infarct size, and increased 5‐year mortality.
Autoimmunity has been considered to contribute to atherosclerosis.
In fact, it seems that both cellular and humoral immune systems are
involved in the development and progression of atherosclerosis.
Several studies have demonstrated autoimmunity related micro
vascular dysfunction caused by increased sympathetic outflow, increased
oxidative stress, increased endothelin‐1 levels, and reduced bioavailability
of nitric oxide in response to shear stress. Nevertheless, coronary flow
reserve, which has been considered as a useful diagnostic index for both
functional and physiologic assessment of coronary circulation, has been
demonstrated to be impaired in several autoimmune diseases, including
systemic sclerosis, and rheumatoid arthritis (RA).
Rheumatoid factor (RF), an antibody against the Fc portion of
immunoglobulin G, has been implicated to have an association with
atherosclerosis. RF is observed not only in RA, but also in other rheumatic
and inflammatory diseases, including Sjogren’s syndrome, systemic lupus
erythematous, and poly dermatomyositis. In addition, positive reactions of
RF can be observed in up to 5% and in up to 25% of healthy young and
elderly population, respectively. RF is associated not only with an
increased likelihood of developing coronary artery disease but also with an
increased cardiovascular mortality in healthy subjects.
Although the association between autoimmunity and no-reflow
phenomenon has not been addressed in the literature, these patients
demonstrate increased rates of poor coronary flow after elective and
primary PCIs.